| First Author | Anderson GA | Year | 2015 |
| Journal | PLoS One | Volume | 10 |
| Issue | 9 | Pages | e0137175 |
| PubMed ID | 26340748 | Mgi Jnum | J:243008 |
| Mgi Id | MGI:5907416 | Doi | 10.1371/journal.pone.0137175 |
| Citation | Anderson GA, et al. (2015) Cardiovascular Patterning as Determined by Hemodynamic Forces and Blood Vessel Genetics. PLoS One 10(9):e0137175 |
| abstractText | BACKGROUND: Vascular patterning depends on coordinated timing of arteriovenous specification of endothelial cells and the concomitant hemodynamic forces supplied by the onset of cardiac function. Using a combination of 3D imaging by OPT and embryo registration techniques, we sought to identify structural differences between three different mouse models of cardiovascular perturbation. RESULTS: Endoglin mutant mice shared a high degree of similarity to Mlc2a mutant mice, which have been shown to have a primary developmental heart defect causing secondary vessel remodeling failures. Dll4 mutant mice, which have well-characterized arterial blood vessel specification defects, showed distinct differences in vascular patterning when compared to the disruptions seen in Mlc2a-/- and Eng-/- models. While Mlc2a-/- and Eng-/- embryos exhibited significantly larger atria than wild-type, Dll4-/- embryos had significantly smaller hearts than wild-type, but this quantitative volume decrease was not limited to the developing atrium. Dll4-/- embryos also had atretic dorsal aortae and smaller trunks, suggesting that the cardiac abnormalities were secondary to primary arterial blood vessel specification defects. CONCLUSIONS: The similarities in Eng-/- and Mlc2a-/- embryos suggest that Eng-/- mice may suffer from a primary heart developmental defect and secondary defects in vessel patterning, while defects in Dll4-/- embryos are consistent with primary defects in vessel patterning. |
